​No prior work has directly compared the impacts of transcranial photobiomodulation (tPBM) and transcranial magnetic stimulation (TMS) on the human brain. This within-subjects pilot study compares the effects of tPBM and TMS of human somatomotor cortex on brain structural and functional connectivity.  . . .

​​Thus, tPBM may be superior to TMS at inducing changes in connected nodes in the somatomotor cortex, although further research is warranted to explore the potential therapeutic benefits and clinical utility of tPBM.

​Abstract

​The human brain is an energetically costly organ, consuming 20-25% of all biochemical energy produced in the body, despite comprising only 2-3% of total body mass.

Most energy in the brain is consumed to support synaptic neurotransmission, which is the primary means of neuron-to-neuron communication between.

This energy is in the form of adenosine triphosphate (ATP), and within neural cells, nearly all ATP is produced by mitochondria via the process of oxidative phosphorylation (OXPHOS).

To ensure that ATP is readily available, mitochondria are trafficked to areas of greater energy use, such as neuronal synapses.

The balance between energetic supply and synaptic communication is essential for proper brain functioning.

This chapter begins with a brief introduction to key features of neuronal synapses and mitochondrial energy production in the cerebral cortex.

Next, the tight and bidirectional coupling of neuronal synaptic activity and mitochondrial OXPHOS is examined from functional, ultrastructural, and molecular perspectives.

​The effects of brain and non-brain organ system perturbations on synaptic-mitochondrial coupling are then examined within the context of (1) primary brain disorders, such as schizophrenia and bipolar disorder, and (2) primary peripheral disorders, such as diabetes and obesity.

​Finally, a discussion of potential intervention strategies that may restore neural communication and mitochondrial bioenergetics, within the framework of the brain-body connection, is provided.

Alterations in these protein pathways persisted into childhood, and dysregulation of GAPDH, SELENBP1, and BLVRB proteins were evident in both cord blood and in serum from pre-pubertal children with Autism

 Our study provides a mechanistic framework linking genetic risk to brain protein dysregulation and proposes tractable therapeutic targets for psychiatric disorders.

Traditionally, microglial subtypes characterized physiologically as “reactive” or “activated” have been linked with disease and injury in the brain.

However, morphologically, a recently described microglia category known as “dystrophic,” characterized structurally by fragmented processes and cytoplasmic decay is believed to be more strongly associated with aging and neurodegeneration. 

​Abstract

Maternal trauma influences infant and adult health outcomes and may impact future generations through epigenetic modifications such as DNA methylation (DNAm).

Based on an epigenome-wide association study (EWAS), we identified differentially methylated regions (DMPs): 14 were associated with germline and 21 with direct exposure to violence.  .  .  .

Most DMPs showed the same directionality in DNAm change across germline, prenatal, and direct exposures, suggesting a common epigenetic response to violence.

Additionally, we identified epigenetic age acceleration in association with prenatal exposure to violence in children, highlighting the critical period of in utero development.

This is the first report of an intergenerational epigenetic signature of violence, which has important implications for understanding the inheritance of trauma.